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Cat. No. ARG34809

JAK2 Knockout HCT116 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Large intestine (colon)

  • Disease:

    Carcinoma

The JAK2 Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HCT 116 colorectal carcinoma line, designed to disrupt the JAK2 gene. JAK2 is a non-receptor tyrosine kinase that transduces cytokine receptor signals (e.g., from EPOR and IL-6R) to STAT3 and STAT5, and additionally activates PI3K/AKT and MAPK cascades, promoting expression of oncogenic targets such as MYC. Applications include dissecting JAK2-driven colorectal cancer mechanisms, screening JAK2 inhibitors, and profiling downstream signaling. Typical assays encompass western blotting, RT-qPCR, proliferation and apoptosis measurements, and functional migration studies.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HCT 116

    Sex of Donor

    Male

    Age

    Adult

    Derived From Site

    In situ; Colon

    Gene Name

    JAK2

    Gene Identifier

    NCBI Gene ID 3717

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    McCoy's 5A

    Supplement(s)

    10% Fetal Bovine Serum, 1% Penicillin-Streptomycin Solution

    Temperature

    37°C

    Atmosphere

    5% CO₂

  • Quality Control

    Sterility testing

    The bacterial, yeast, and fungi are not detected in these cells by daily monitor.

    Mycoplasma testing

    Negative for mycoplasma through PCR analysis

  • Disclaimer

    Intended Use

    This product is intended for laboratory in vitro use only. lt is not intended for diagnostic, therapeutic, or clinical applications.

    Disclaimer

    Ascent Research endeavors to provide accurate and up-to-date product information. However, no warranties or representations are made regarding its completeness or reliability. References to scientific literature and patents are for informational purposes only, and the customer assumes sole responsibility for verifying their accuracy.

    By accepting this product, the customer acknowledges and agrees to assume all risks associated with its receipt, handling, storage, disposal, and use, including compliance with all applicable safety and environmental regulations and precautions. Relevant laws, regulations, and ethical guidelines must be followed in conducting any research, modifications, or derivatives derived from this product.

    This product is provided "AS IS", and except as expressly stated herein, Ascent Research disclaims all other warranties, express or implied. Under no circumstances shall Ascent Research, its affiliates, or representatives be liable for indirect, incidental, consequential, or punitive damages arising from the use of this material. While Ascent Research employs rigorous quality control measures, we shall not be held responsible for damages resulting from misidentification or misinterpretation of the provided materials.

Description

The JAK2 Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population engineered for loss-of-function studies of the JAK2 gene in the HCT 116 colorectal carcinoma line. The polyclonal format, generated by CRISPR/Cas9-mediated gene disruption, comprises a heterogeneous mix of edited cells, minimizing clonal bias and enabling robust assessment of JAK2-dependent phenotypes. This product is designed for advanced research requiring disruption of JAK-STAT signaling in a well-characterized colorectal cancer model.

HCT 116 is a human colorectal carcinoma epithelial cell line derived from a male patient, widely employed as a model for colorectal cancer biology and drug discovery. The cells retain key oncogenic features, including deregulated proliferative signaling and apoptotic resistance, making them a relevant host for investigating oncogenic kinase networks. Their adherent growth and well-annotated genome facilitate molecular analyses following gene perturbation.

JAK2 encodes a non-receptor tyrosine kinase that transduces signals from cytokine receptors such as EPOR, MPL, and IL-6R. Upon activation, JAK2 phosphorylates STAT3 and STAT5, which dimerize and regulate transcription of genes like MYC and CCND1; it additionally activates PI3K/AKT and MAPK/ERK cascades. Negative regulators include SOCS1, SOCS3, PTPN6, and PIAS proteins. In HCT 116 cells, JAK2 mediates cytokine-driven proliferation and survival, and its knockout abrogates downstream STAT and AKT/ERK activation.

Aberrant JAK2 activity contributes to colorectal tumor growth and inflammatory signaling. The JAK2 knockout polyclonal cells enable dissection of JAK2??s role in cytokine-induced oncogenesis, independent of clonal artifacts. This model supports screening of JAK2 inhibitors and evaluation of pathway-specific dependencies in a solid tumor context, aiding the development of targeted therapies for colorectal cancer.

Research applications include western blotting and phospho-flow cytometry for JAK2/STAT pathway analysis, RT-qPCR and RNA-seq for gene expression profiling, and functional assays such as MTT proliferation, Annexin V apoptosis, colony formation, and migration/invasion tests. Co-immunoprecipitation and luciferase reporter assays further delineate JAK2 interaction networks and transcriptional responses. For additional technical support, please contact Ascent Research.

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